Prl8a2-flox 基因敲除小鼠

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产品名称

Prl8a2-flox 基因敲除小鼠

产品编号

S-CKO-02113

品系全称

C57BL/6JCya-Prl8a2em1flox/Cya

品系背景

C57BL/6JCya

品系编号

CKOCMP-13529-Prl8a2-B6J-VA

品系状态

使用本品系发表的文献需注明: Prl8a2-flox 基因敲除小鼠 mice (Strain S-CKO-02113) were purchased from Cyagen.
交付类型
周龄
性别
基因型
数量
cKO小鼠库模型

基本信息

基因研究概述

质控标准

基因
基因全称
prolactin family 8, subfamily a, member 2
基因别称
D/tPRP,DPRP,Dtprp,Ghd11,mdPRP
染色体号
Chr 13 (Mouse)
转录本 ID
NCBI: NM_010088 | Ensembl: ENSMUST00000018403
修饰方式
条件性基因敲除
靶向范围
Exon 2~3
敲除长度
~1.8 kb
品系说明
该品系是基于策略设计时的数据库信息制作而成,建议您在购买前查询最新的数据库和相关文献,以获取最准确的表型信息。
表型提示
MGI:894281Mice homozygous for a null allele exhibit reduced pregnancy success when exposed to hypoxic conditions.
PRL8A2,也称为decidual prolactin-related protein (dPRP),是一种属于prolactin家族的蛋白质。PRL8A2主要在子宫的蜕膜中表达,并参与妊娠相关的适应性反应,如缺氧适应[1]。PRL8A2的表达和功能受到多种因素的调控,包括激素、细胞因子和转录因子等[2,3,4,5,6,7,8,9,10]。

在蜕膜化过程中,PRL8A2的表达受到多种因素的调控。例如,Hmgb3通过靶向Ptn来诱导子宫间质细胞的分化,进而促进PRL8A2的表达[3]。TAZ作为一种Hippo信号通路的效应因子,可以促进蜕膜细胞的增殖和分化,并通过Nrf2/ARE/Foxo1信号通路来减轻氧化损伤,从而保护蜕膜细胞免受氧化应激的损害[6]。Hmgn1和Hmgn3作为高迁移率组蛋白家族的成员,可以促进蜕膜化标记基因PRL8A2和PRL3c1的表达,并参与调控蜕膜化过程中的基因表达和细胞分化[7,9]。此外,研究还发现,Sorbs1可能是一个与女性不孕症相关的候选基因,其敲低可以抑制蜕膜化标记基因PRL8A2的表达[8]。

PRL8A2的功能和表达受到多种因素的调控,并在蜕膜化过程中发挥重要作用。进一步研究PRL8A2的调控机制和功能,有助于深入理解蜕膜化过程的生物学机制,并为相关疾病的治疗和预防提供新的思路和策略。

参考文献:
1. Alam, S M Khorshed, Konno, Toshihiro, Soares, Michael J. . Identification of target genes for a prolactin family paralog in mouse decidua. In Reproduction (Cambridge, England), 149, 625-32. doi:10.1530/REP-15-0107. https://pubmed.ncbi.nlm.nih.gov/25926690/
2. Dickson, Mackenzie J, Oh, Yeongseok, Gruzdev, Artiom, Wu, San-Pin, DeMayo, Francesco J. 2022. Inserting Cre recombinase into the Prolactin 8a2 gene for decidua-specific recombination in mice. In Genesis (New York, N.Y. : 2000), 60, e23473. doi:10.1002/dvg.23473. https://pubmed.ncbi.nlm.nih.gov/35475540/
3. Wang, Kai, Yin, Yun-Hou, Yang, Zhan-Qing, Guo, Bin, Yue, Zhan-Peng. 2018. Hmgb3 Induces the Differentiation of Uterine Stromal Cells Through Targeting Ptn. In Reproductive sciences (Thousand Oaks, Calif.), 26, 891-899. doi:10.1177/1933719118792098. https://pubmed.ncbi.nlm.nih.gov/30081728/
4. Wang, Peng-Chao, Yang, Zhen-Shan, Gu, Xiao-Wei. . Effect of Aurora kinase B on polyploidy and decidualization in mouse uterus. In American journal of reproductive immunology (New York, N.Y. : 1989), 90, e13793. doi:10.1111/aji.13793. https://pubmed.ncbi.nlm.nih.gov/37881124/
5. Kang, Jinwen, Liu, Yingnan, Zhang, Yu, Wu, Yao, Su, Renwei. 2022. The Influence of the Prolactins on the Development of the Uterus in Neonatal Mice. In Frontiers in veterinary science, 9, 818827. doi:10.3389/fvets.2022.818827. https://pubmed.ncbi.nlm.nih.gov/35252420/
6. Yu, Hai-Fan, Zheng, Lian-Wen, Yang, Zhan-Qing, Yue, Zhan-Peng, Guo, Bin. 2021. TAZ as a novel regulator of oxidative damage in decidualization via Nrf2/ARE/Foxo1 pathway. In Experimental & molecular medicine, 53, 1307-1318. doi:10.1038/s12276-021-00655-2. https://pubmed.ncbi.nlm.nih.gov/34497345/
7. Li, Dang-Dang, Yang, Zhan-Qing, Guo, Chuan-Hui, Guo, Bin, Yue, Zhan-Peng. . Hmgn1 acts downstream of C/EBPβ to regulate the decidualization of uterine stromal cells in mice. In Cell cycle (Georgetown, Tex.), 14, 3461-74. doi:10.1080/15384101.2015.1093704. https://pubmed.ncbi.nlm.nih.gov/26566865/
8. Liu, Ji-Long, Wang, Tong-Song, Zhao, Miao. 2016. Genome-Wide Association Mapping for Female Infertility in Inbred Mice. In G3 (Bethesda, Md.), 6, 2929-35. doi:10.1534/g3.116.031575. https://pubmed.ncbi.nlm.nih.gov/27449513/
9. Li, Dang-Dang, Guo, Chuan-Hui, Yue, Liang, Guo, Bin, Yue, Zhan-Peng. 2015. Expression, regulation and function of Hmgn3 during decidualization in mice. In Molecular and cellular endocrinology, 413, 13-25. doi:10.1016/j.mce.2015.05.038. https://pubmed.ncbi.nlm.nih.gov/26112184/
10. Hu, Min, Zhang, Yuehui, Guo, Xiaozhu, Shao, Linus R, Billig, Håkan. 2019. Hyperandrogenism and insulin resistance induce gravid uterine defects in association with mitochondrial dysfunction and aberrant reactive oxygen species production. In American journal of physiology. Endocrinology and metabolism, 316, E794-E809. doi:10.1152/ajpendo.00359.2018. https://pubmed.ncbi.nlm.nih.gov/30860876/